Recovering from stroke with proper nutrition

Nutrition and Dietary Supplements

You should seek conventional medical treatment for stroke. You should use complementary and alternative therapies only under the supervision of a health care provider. Supplements can have negative effects on certain segments of the population, and can interact negatively with prescription medications. Make sure all of your medical providers are aware of any supplements you are considering taking.

Potentially beneficial nutritional supplements include the following:

Alpha-lipoic acid. Alpha-lipoic acid works together with other antioxidants, such as vitamins C and E. It is important for growth, helps prevent cell damage, and helps the body rid itself of harmful substances. Because alpha-lipoic acid can pass easily into the brain, it has protective effects on brain and nerve tissue, and shows promise as a treatment for stroke and other brain disorders involving free radical damage. Animals treated with alpha-lipoic acid, for example, suffered less brain damage and had a four times greater survival rate after a stroke than the animals who did not receive this supplement, especially when alpha-lipoic acid is combined with vitamin E. While animal studies are encouraging, more research is needed to understand whether this benefit applies to people as well.

Calcium.. In a population-based study (one in which large groups of people are followed over time), women who took in more calcium, both through the diet and supplements, were less likely to have a stroke over a 14-year period. More research is needed to fully assess the strength of the connection between calcium and risk of stroke.

Folic Acid, Vitamin B6, Vitamin B12, and Betaine. Many clinical studies indicate that patients with elevated levels of the amino acid homocysteine are up to 2.5 times more likely to suffer from a stroke than those with normal levels. Homocysteine levels are strongly influenced by dietary factors, particularly vitamin B9 (folic acid), vitamin B6, vitamin B12, and betaine. These substances help break down homocysteine in the body. Some studies have even shown that healthy individuals who consume higher amounts of folic acid and vitamin B6 are less likely to develop atherosclerosis than those who consume lower amounts of these substances. One study found that lowering homocysteine with folic acid and vitamins B6 and B12 reduced the overall risk of stroke, but not stroke severity or disability. Despite these findings, the American Heart Association (AHA) reports that there is insufficient evidence to suggest that supplementation with betaine and B vitamins reduce the risk of atherosclerosis, or that taking these supplements prevents the development or recurrence of heart disease. The AHA does not currently recommend population-wide homocysteine screening, and suggests that folic acid, as well as vitamin B6, B12, and betaine requirements be met through diet alone. Individuals at high risk for developing atherosclerosis, however, should be screened for blood levels of homocysteine. If elevated levels are detected, a provider may recommend supplementation.

Magnesium. Population-based information suggests that people with low magnesium in their diet may be at greater risk for stroke. Some preliminary scientific evidence suggests that magnesium sulfate may be helpful in the treatment of a stroke or TIA. More research is needed to know for certain if use of this mineral following a stroke or TIA is helpful. Magnesium may lower blood pressure and potentially interact with some heart medicines.

Omega-3 Fatty Acids. Strong evidence from population-based studies suggests that omega-3 fatty acid intake (primarily from fish) helps protect against stroke caused by plaque buildup and blood clots in the arteries that lead to the brain. In fact, eating at least 2 servings of fish per week can reduce the risk of stroke by as much as 50%. However, people who eat more than 3 grams of omega-3 fatty acids per day (equivalent to 3 servings of fish per day) may be at an increased risk for hemorrhagic stroke, a potentially fatal type of stroke in which an artery in the brain leaks or ruptures. Omega-3 fatty acids may increase the chances of bleeding, especially in those taking anticoagulant medications, such as warfarin (Coumadin) or even aspirin.

The FDA recommends that pregnant women and women of childbearing age, who may become pregnant, avoid large predatory fish such as shark, tuna, and swordfish. These fish have much higher levels of methyl mercury than other commonly consumed fish. Since the fetus may be more susceptible than the mother to the adverse effects of methyl mercury, FDA experts say that it is prudent to minimize the consumption of fish that have higher levels of methyl mercury.

Potassium. Although low levels of potassium in the blood may be associated with stroke, taking potassium supplements does not seem to reduce the risk of having a stroke.

Vitamin C. Having low levels of vitamin C contributes to the development of atherosclerosis and other damage to blood vessels and the consequences, such as stroke. Vitamin C supplements may also improve cognitive function if you have suffered from multiple strokes.

Vitamin E. Eating plenty of foods rich in vitamin E, along with other antioxidants like vitamin C, selenium, and carotenoids, reduces your risk for stroke. In addition, low levels of vitamin E in the blood may be associated with risk of dementia (memory impairment) following stroke. Animal studies also suggest that vitamin E supplements, possibly in combination with alpha-lipoic acid, may reduce the amount of brain damaged if taken prior to the actual stroke. Researchers suggest testing this theory in people who are at high risk for stroke. Thus far, however, some large, well-designed studies of people suggest that it is safest and best to obtain this antioxidant via food sources, and that supplements do not provide any added benefit.

Others. Additional supplements that require further research but may be useful as part of the treatment or prevention of stroke include:

  • Coenzyme Q10 (CoQ10). CoQ10 works as an antioxidant and may reduce damage following a stroke. CoQ10 may increase the ability of the blood to clot and therefore interfere with some blood-thinning medicines, such as warfarin (Coumadin) and others.
  • Selenium. Low levels can worsen atherosclerosis and its consequences. However, scientists do not know whether taking selenium supplements will help.


The use of herbs is a time-honored approach to strengthening the body and treating disease. Herbs, however, contain active substances that can trigger side effects and interact with other herbs, supplements, or medications. For these reasons, you should take herbs only under the supervision of a health care provider knowledgeable in the field.

Bilberry (Vaccinium myrtillus). A close relative of the cranberry, bilberry fruits contain flavonoid compounds called anthocyanidins. Flavonoids are plant pigments that have excellent antioxidant properties. This means that they scavenge damaging particles in the body known as free radicals and may help prevent a number of long-term illnesses, such as heart disease. Bilberry may slow blood clotting and therefore may increase the risk of bleeding in people who take blood-thinning medications, such as warfarin (Coumadin), aspirin, and others.

Garlic (Allium sativum). Clinical studies suggest that fresh garlic and garlic supplements may prevent blood clots and destroy plaque. Blood clots and plaque block blood flow and contribute to the development of heart attack and stroke. Garlic may also be beneficial for reducing risk factors for heart disease and stroke like high blood pressure, high cholesterol, and diabetes. Homocysteine, similar to cholesterol, may contribute to increasing amounts of blood clots and plaque in blood vessels. If you take aspirin or other blood thinners like warfarin (Coumadin), ACE inhibitors (a class of blood pressure medications), sulfonylureas for diabetes, birth control medications, medications for HIV, or statins for high cholesterol, talk to your doctor before using garlic supplements.

Ginkgo (Ginkgo biloba). Gingko may reduce the likelihood of dementia following multiple strokes (often called multi-infarct dementia) by preventing blood clot formation. Most providers choose to use medications for this effect rather than herbs. Ginkgo may also decrease the amount of brain damage following a stroke. While animal studies support these possible benefits of ginkgo, more research is needed. Also, ginkgo should not be used with blood-thinning medications, such as warfarin (Coumadin), aspirin, and others, unless specifically instructed by your provider.

Ginseng (Panax ginseng). Asian ginseng may decrease endothelial cell dysfunction. Endothelial cells line the inside of blood vessels. When these cells are disturbed, it may lead to a heart attack or stroke. The potential for ginseng to quiet down the blood vessels may prove to be protective against these conditions. More research is needed. Ginseng can have stimulating effects that may be harmful to certain people. Ginseng may also thin your blood and, therefore, should be used only under the supervision of a doctor, particularly if you are taking blood-thinning medication, such as warfarin (Coumadin), aspirin, and others.

Turmeric (Curcuma longa). Early studies suggest that turmeric may prevent heart attack or stroke. Animal studies have shown that an extract of turmeric lowered cholesterol levels and inhibited the oxidation of LDL (bad) cholesterol. This is helpful because oxidized LDL deposits in the walls of blood vessels and contributes to the formation of atherosclerotic plaque and other damage to the vessels. Turmeric may also prevent platelet build up along the walls of an injured blood vessel. Platelets collecting at the site of a damaged blood vessel cause blood clots to form and contribute to blocking the artery as well. Turmeric may also thin your blood and, therefore, should only be used under the supervision of a provider, particularly if you are taking blood-thinning medications, such as warfarin (Coumadin), aspirin, and others. More research is needed to determine whether these effects apply to people.


Although an experienced homeopath might prescribe a regimen for treating stroke that includes one of the remedies listed below, the scientific evidence to date does not confirm the value of homeopathy for this purpose.

  • Acontitum napellus. For numbness or paralysis after a cerebral accident.
  • Belladonna. For stroke that leaves the person very sensitive to any motion, with vertigo and trembling.
  • Kali bromatum. For stroke resulting in restlessness, wringing of the hands or other repeated gestures, insomnia, and night terrors.
  • Nux vomica. For cerebral accident with paresis (muscular weakness caused by disease of the nervous system), expressive aphasia (language disorder), convulsions, and great irritability.


Many studies have been conducted on the effects of acupuncture during stroke rehabilitation. These studies show that acupuncture reduces hospital stays and improves recovery speed. Acupuncture has been shown to help stroke patients regain motor and cognitive skills and to improve their ability to manage daily functioning. Based on the available data, the National Institutes of Health recommend acupuncture as an alternative or supplemental therapy for stroke rehabilitation. In general, the evidence indicates that acupuncture is most effective when initiated as soon as possible after a stroke occurs, however positive outcomes have been found for acupuncture started as late as 6 months following a stroke.

People who have suffered a stroke often have a deficiency of qi in the liver meridian and a relative excess in the gallbladder meridian. In addition to a primary needling treatment on the liver meridian and the supporting kidney meridians, moxibustion (a technique in which the herb mugwort is burned over specific acupuncture points) may be used to enhance therapy. Treatment may also include performing acupuncture on affected limbs. Certain scalp acupuncture techniques that have been developed by Chinese, Korean, and Japanese practitioners also show promise.


Chiropractors do not treat stroke, and high velocity manipulation of the upper spine is considered inappropriate in individuals who are taking blood-thinning medications, or other medications used to reduce the risk of stroke. It should also be noted that chiropractic spinal manipulation of the neck is associated with an exceedingly small risk of causing stroke (reports range from 1 per 400,000 to 1 per 2,000,000).

Traditional Chinese Medicine

In Traditional Chinese Medicine, there are reports of more than 100 substances that have been used to treat stroke. In fact, pharmacologic research of these substances focuses on understanding the ingredients and their mechanisms of action in order to develop new drugs.

Prognosis and Complications

There are many possible complications associated with stroke, including:

  • Seizures
  • Paralysis
  • Cognitive (thinking) deficits
  • Speech problems
  • Emotional difficulties
  • Daily living problems
  • Pain
  • Memory deficits

Many people begin to recover from a stroke almost immediately after it has occurred.

The recovery process is most rapid in the first 3 months after a stroke, but improvement will continue for 6 months to a year. Many stroke survivors even report that they slowly continue to regain function for years after their stroke. It is very important not to lose hope.

Connie’s comments: I would start with bananas, figs, oranges, avocado, walnut, fish, olive oil, colored foods and soups with bone marrow from beef, chicken or turkey.  I prefer supplements of Lifepak and AGELOC at:

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Menopause and Type 2 diabetes

meno t2dm

Diabetes and menopause

Menopause is the phase of life after your periods have stopped and your estrogen levels decline. The hormones estrogen and progesterone affect how your cells respond to insulin. After menopause, changes in your hormone levels can trigger fluctuations in your blood sugar level. Up you calcium, magnesium, Vitamin B complex, E, D, C, K, zinc and other nutrients.

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Watery Diarrhea from virus/bacteria

Acute Diarrhea. Most cases of acute, watery diarrhea are caused byviruses (viral gastroenteritis). The most common ones in children are rotavirus and in adults are norovirus (this is sometimes called “cruise ship diarrhea” due to well publicized epidemics). Bacteria are a common cause of traveler’s diarrhea.

By Dr Blanca Ochoa

Acute diarrhea is one of the most commonly reported illnesses in the United States, second only to respiratory infections. Worldwide, it is a leading cause of mortality in children younger than four years old, especially in the developing world. Diarrhea that lasts less than 2 weeks is termed acute diarrhea. Persistent diarrhea lasts between 2 and 4 weeks. Chronic diarrhea lasts longer than 4 weeks.Symptoms

Diarrheal stools are those that take shape of the container, so they are often described as loose or watery. Some people consider diarrhea as an increase in the number of stools, but stool consistency is really the hallmark. Associated symptoms can include abdominal cramps fever, nausea, vomiting, fatigue and urgency. Chronic diarrhea can be accompanied by weight loss, malnutrition, abdominal pain or other symptoms of the underling illness. Clues for organic disease are weight loss, diarrhea that wakes you up at night, or blood in the stools. These are signs that your doctor will want to do a thorough evaluation to determine the cause of your symptoms. Also tell your doctor if you have a family history of celiac disease, inflammatory bowel disease (IBD), have unintentional weight loss, fever, abdominal cramping or decreased appetite. Tell your doctor if you experience bulky, greasy or very bad smelling stools.

Causes – Acute Diarrhea

Most cases of acute, watery diarrhea are caused by viruses (viral gastroenteritis). The most common ones in children are rotavirus and in adults are norovirus (this is sometimes called “cruise ship diarrhea” due to well publicized epidemics). Bacteria are a common cause of traveler’s diarrhea.

Causes – Chronic Diarrhea

Chronic diarrhea is classified as fatty or malabsorption, inflammatory or most commonly watery. Chronic bloody diarrhea may be due to inflammatory bowel disease (IBD), which is ulcerative colitis or Crohn’s disease. Other less common causes include ischemia of the gut, infections, radiation therapy and colon cancer or polyps. Infections leading to chronic diarrhea are uncommon, with the exception of parasites.

The two major causes of fatty or malabsorptive diarrhea are impaired digestion of fats due to low pancreatic enzyme levels and impaired absorption of fats due to small bowel disease. These conditions interfere with the normal processing of fats in the diet. The former is usually due to chronic pancreatitis which is a result of chronic injury to the pancreas. Alcohol damage to the pancreas is the most common cause of chronic pancreatitis in the United States. Other causes of chronic pancreatitis include cystic fibrosis, hereditary pancreatitis, trauma to the pancreas and pancreatic cancer.

The most common small bowel disease in the U.S. is celiac disease, also called celiac sprue. Crohn’s disease can also involve the small bowel. Whipple’s disease, tropical sprue, and eosinophilic gastroenteritis are some of the rare conditions that can lead to malabsorption diarrhea.

There are many causes of watery diarrhea, including carbohydrate malabsorption such as lactose, sorbitol, and fructose intolerance. Symptoms of abdominal bloating and excessive gas after consuming dairy products suggests lactose intolerance. This condition is more common in African-Americans and Asian-Americans. Certain soft drinks, juices, dried fruits and gums contain sorbitol and fructose, which can lead to watery diarrhea in people with sorbitol and fructose intolerance. Diarrhea is a frequent side effect of antibiotics. Certain other medications such as NSAIDs, antacids, antihypertensives, antibiotics and antiarrhythmics can have side effects leading to diarrhea.

Parasitic intestinal infections such as giardiasis can cause chronic diarrhea. Diabetes mellitus may be associated with diarrhea due to nerve damage and bacterial overgrowth; this occurs mainly in patients with long-standing, poorly-controlled diabetes.

Irritable bowel syndrome (IBS) is a condition often associated with diarrhea, constipation or more frequently alternating diarrhea and constipation. Other common symptoms are bloating, abdominal pain relieved with defecation and a sense of incomplete evacuation.

Risk Factors

Exposure to infectious agents is the major risk factor for acute diarrhea. Bacteria and viruses are often transmitted by the fecal-oral route, so hand washing and hygiene are important to prevent infection. Soap and water are better because alcohol-based hand sanitizers may not kill viruses. Medications such as antibiotics and drugs that contain magnesium products are also common offenders. Recent dietary changes can also lead to acute diarrhea. These including intake of coffee, tea, colas, dietetic foods, gums or mints that contain poorly absorbable sugars. Acute bloody diarrhea suggests a bacterial cause like Campylobacter, Salmonella or Shigella or Shiga-toxin E. coli. Traveler’s diarrhea is common in those who travel to developing countries and results from exposure to bacterial pathogens most commonly enterotoxigenic E. coli. The best method of prevention is to avoid eating and drinking contaminated or raw foods and beverages.


Most episodes of acute diarrhea resolve quickly without antibiotic therapy and with simple dietary modifications. See a doctor if you feel ill, have bloody diarrhea, severe abdominal pain or diarrhea lasting more than 48 hours. In patients with mild acute diarrhea, no laboratory evaluation is needed because the illness generally resolves quickly. Your doctor may perform stool tests for bacteria and parasites if your diarrhea is severe or bloody or if you traveled to an area where infections are common. If you have severe diarrhea, blood tests will be helpful to guide replacement of fluid and electrolytes and minerals such as magnesium, potassium and zinc that can become depleted.

If you have chronic diarrhea, your doctor will want to further assess etiologic factors or complications of diarrhea by obtaining several tests. These can include a blood count to look for anemia and infections, an electrolyte and kidney function panel to assess for electrolyte abnormalities and renal insufficiency, and albumin to assess your nutritional status.

A stool sample may help define the type of diarrhea. The presence of fat, microscopic amounts of blood, and white blood cells will help determine if a fatty, inflammatory, or watery diarrhea is present. A bacterial culture and ova/parasite studies of a stool specimen will also help determine if an infectious etiology is present.

Endoscopic examination of the colon with flexible sigmoidoscopy or colonoscopy and upper endoscopy are helpful in detecting the etiology of chronic diarrhea, as this allows direct examination of the bowel mucosa and the ability to obtain biopsies for microscopic evaluation. Double-balloon enteroscopy and capsule endoscopy are sometimes used to examine the mucosa of the small intestine that lies beyond the reach of conventional endoscopes.

Radiographic studies such as an upper GI series or barium enema are not routinely performed in the evaluation of chronic diarrhea, and have largely been replaced by cross-sectional imaging. Ultrasound and CT scan of the abdomen can be helpful to evaluate the bowel, pancreas and other intra-abdominal organs.

Treating Acute Diarrhea

It is important to take plenty of fluid with sugar and salt to avoid dehydration. Salt and sugar together in a beverage help your intestine absorb fluids. Milk and dairy products should be avoided for 24 to 48 hours as they can make diarrhea worse. Initial dietary choices when refeeding should begin with soups and broth.

Anti-diarrheal drug therapy can be helpful to control severe symptoms, and includes bismuth subsalicylate and antimotility agents such as loperamide. These, however, should be avoided in people with high fever or bloody diarrhea as they can worsen severe colon infections and in children because the use of anti-diarrheals can lead to complications of hemolytic uremic syndrome in cases of Shiga-toxin E. coli (E. coli 0157:H7).

Your doctor may prescribe antibiotics if you have high fever, dysentery, or moderate to severe traveler’s diarrhea. Some infections such as Shigella always require antibiotic therapy.

Treatment of chronic diarrhea depends on the etiology of the chronic diarrhea. Often, empiric treatment can be provided for symptomatic relief, when a specific diagnosis is not reached, or when a diagnosis that is not specifically treatable is reached.

Antimotility agents such as loperamide are the most effective agents for the treatment of chronic diarrhea. They reduce symptoms as well as stool weight. Attention should be paid to replacing any mineral and vitamin deficiencies, especially calcium, potassium, magnesium and zinc.


Calcium in our foods and bodies


The effects of calcium on human cells are specific, meaning that different types of cells respond in different ways. However, in certain circumstances, its action may be more general. Ca2+ ions are one of the most widespread second messengers used in signal transduction. They make their entrance into the cytoplasm either from outside the cell through the cell membrane via calcium channels (such as Calcium-binding proteins or voltage-gated calcium channels), or from some internal calcium storages such as the endoplasmic reticulum[3] and mitochondria. Levels of intracellular calcium are regulated by transport proteins that remove it from the cell. For example, the sodium-calcium exchanger uses energy from the electrochemical gradient of sodium by coupling the influx of sodium into cell (and down its concentration gradient) with the transport of calcium out of the cell. In addition, the plasma membrane Ca2+ ATPase (PMCA) obtains energy to pump calcium out of the cell by hydrolysing adenosine triphosphate (ATP). In neurons, voltage-dependent, calcium-selective ion channels are important for synaptic transmission through the release of neurotransmitters into the synaptic cleft by vesicle fusion of synaptic vesicles.

Calcium’s function in muscle contraction was found as early as 1882 by Ringer. Subsequent investigations were to reveal its role as a messenger about a century later. Because its action is interconnected with cAMP, they are called synarchic messengers. Calcium can bind to several different calcium-modulated proteins such as troponin-C (the first one to be identified) and calmodulin, proteins that are necessary for promoting contraction in muscle.

In the endothelial cells which line the inside of blood vessels, Ca2+ ions can regulate several signaling pathways which cause the smooth muscle surrounding blood vessels to relax.[citation needed] Some of these Ca2+-activated pathways include the stimulation of eNOS to produce nitric oxide, as well as the stimulation of Kca channels to efflux K+ and cause hyperpolarization of the cell membrane. Both nitric oxide and hyperpolarization cause the smooth muscle to relax in order to regulate the amount of tone in blood vessels.[7] However, dysfunction within these Ca2+-activated pathways can lead to an increase in tone caused by unregulated smooth muscle contraction. This type of dysfunction can be seen in cardiovascular diseases, hypertension, and diabetes.

Calcium: magnesium ratio is 60:40 and always taken with Vit C, Vit D3 and zinc and in afternoon while iron rich foods is eaten in the morning since calcium and iron cancels each other out.

Hypocalcemia and Sepsis

hypoHypocalcemia varies from an asymptomatic biochemical abnormality to a life-threatening disorder, depending on the duration, severity, and rapidity of development. Hypocalcemia is caused by loss of calcium from or insufficient entry of calcium into the circulation.

Hypoparathyroidism is the most common cause of hypocalcemia and often develops because of surgery in the central neck requiring radical resection of head and neck cancers. It develops in 1% to 2% of patients after total thyroidectomy.

The hypocalcemia may be transient, permanent, or intermittent, as with vitamin D deficiency during the winter. Autoimmune hypoparathyroidism is seen as an isolated defect or as part of polyglandular autoimmune syndrome type I in association with adrenal insufficiency and mucocutaneous candidiasis. Most of these patients have autoantibodies directed against the calcium-sensing receptor. Congenital causes of hypocalcemia include activating mutations of calcium-sensing receptor, which has reset the calcium–parathyroid hormone (PTH) relation to a lower serum calcium level. Mutations affecting intracellular processing of the pre-pro-PTH molecule are also described and lead to hypoparathyroidism, hypocalcemia, or both. Finally, some cases are associated with hypoplasia or aplasia of the parathyroid glands; the best known is DiGeorge syndrome.

Pseudohypoparathyroidism is a group of disorders with postreceptor resistance to PTH. One classic variant is Albright’s hereditary osteodystrophy, associated with low stature, round facies, short digits, and mental retardation. Hypomagnesemia induces PTH resistance and also affects PTH production. Severe hypermagnesemia (>6 mg/dL) can lead to hypocalcemia by inhibiting PTH secretion. Vitamin D deficiency leads to hypocalcemia when associated with decreased dietary calcium intake. The low calcium level stimulates PTH secretion (secondary hyperparathyroidism), leading to hypophosphatemia.

Rhabdomyolysis and tumor lysis syndrome cause loss of calcium from the circulation when large amounts of intracellular phos-phate are released and precipitate calcium in bone and extraskeletal tissues. A similar mechanism causes hypocalcemia with phosphate administration.

Acute pancreatitis precipitates calcium as a soap in the abdomen, causing hypocalcemia. Hungry bone syndrome is hypocalcemia after surgery for hyperparathyroidism (HPT) in patients with severe prolonged disease (secondary or tertiary HPT in renal failure). Serum calcium is rapidly deposited into the bone. Hungry bone syndrome is rarely seen after correction of longstanding metabolic acidosis or after thyroidectomy for hyperthyroidism.

Several medications (e.g., ethylenediaminetetraacetic acid [EDTA], citrate present in transfused blood, lactate, foscarnet) chelate calcium in the circulation, sometimes producing hypocalcemia in which ionized calcium is decreased, cohereas total calcium may be normal. Extensive osteoblastic skeletal metastases (prostate and breast cancers) may also cause hypocalcemia. Chemotherapy, including cisplatin, 5-fluorouracil, and leucovorin, causes hypocalcemia mediated through hypomagnesemia. Hypocalcemia after surgery can be mediated by the citrate content of transfused blood or by a large volume of fluid administration and hypoalbuminemia. Patients with sepsis demonstrate hypocalcemia usually associated with hypoalbuminemia.

Ionized means charged. Sepsis is the other cause of hypocalcemia (absence of PTH secretion or hypoparathyroidism). Low calcium, high magnesium and low Vitamin D3. Can also be congenital (mutations of CaSR, PTH, and parathyroid aplasia)

Supplementation of calcium 60%, magnesium 40% with zinc, Vitamin D and C and should be taken before eating food rich in iron since iron cancels calcium absorption.

Metabolic pathway provides cues for cancer, aging and health care

metabolic path.JPGIn biochemistry, a metabolic pathway is a linked series of chemical reactions occurring within a cell. The reactants, products, and intermediates of an enzymatic reaction are known as metabolites, which are modified by a sequence of chemical reactions catalyzed by enzymes.[1] In a metabolic pathway, the product of one enzyme acts as the substrate for the next. These enzymes often require dietary minerals, vitamins, and other cofactors to function.

Different metabolic pathways function based on the position within a eukaryotic cell and the significance of the pathway in the given compartment of the cell.[2] For instance, the citric acid cycle, electron transport chain, and oxidative phosphorylation all take place in the mitochondrial membrane. In contrast, glycolysis, pentose phosphate pathway, and fatty acid biosynthesis all occur in the cytosolof a cell.[3]

There are two types of metabolic pathways that are characterized by their ability to either synthesize molecules with the utilization of energy (anabolic pathway) or break down of complex molecules by releasing energy in the process (catabolic pathway).[4] The two pathways complement each other in that the energy released from one is used up by the other. The degradative process of a catabolic pathway provides the energy required to conduct a biosynthesis of an anabolic pathway.[4] In addition to the two distinct metabolic pathways is the amphibolic pathway, which can be either catabolic or anabolic based on the need for or the availability of energy.[5]

Pathways are required for the maintenance of homeostasis within an organism and the flux of metabolites through a pathway is regulated depending on the needs of the cell and the availability of the substrate. The end product of a pathway may be used immediately, initiate another metabolic pathway or be stored for later use. The metabolism of a cell consists of an elaborate network of interconnected pathways that enable the synthesis and breakdown of molecules (anabolism and catabolism)

Glycolysis, Oxidative Decarboxylation of Pyruvate, and Tricarboxylic Acid (TCA) Cycle

Net reactions of common metabolic pathways

Each metabolic pathway consists of a series of biochemical reactions that are connected by their intermediates: the products of one reaction are the substrates for subsequent reactions, and so on. Metabolic pathways are often considered to flow in one direction. Although all chemical reactions are technically reversible, conditions in the cell are often such that it is thermodynamically more favorable for flux to flow in one direction of a reaction. For example, one pathway may be responsible for the synthesis of a particular amino acid, but the breakdown of that amino acid may occur via a separate and distinct pathway. One example of an exception to this “rule” is the metabolism of glucose. Glycolysis results in the breakdown of glucose, but several reactions in the glycolysis pathway are reversible and participate in the re-synthesis of glucose (gluconeogenesis).

  • Glycolysis was the first metabolic pathway discovered:
  1. As glucose enters a cell, it is immediately phosphorylated by ATP to glucose 6-phosphate in the irreversible first step.

  2. In times of excess lipid or protein energy sources, certain reactions in the glycolysis pathway may run in reverse in order to produce glucose 6-phosphate which is then used for storage as glycogen or starch.

  • Metabolic pathways are often regulated by feedback inhibition.
  • Some metabolic pathways flow in a ‘cycle’ wherein each component of the cycle is a substrate for the subsequent reaction in the cycle, such as in the Krebs Cycle (see below).
  • Anabolic and catabolic pathways in eukaryotes often occur independently of each other, separated either physically by compartmentalization within organelles or separated biochemically by the requirement of different enzymes and co-factors.

Catabolic pathway (catabolism)

A catabolic pathway is a series of reactions that bring about a net release of energy in the form of a high energy phosphate bond formed with the energy carriers Adenosine Diphosphate (ADP) and Guanosine Diphosphate (GDP) to produce Adenosine Triphosphate (ATP) and Guanosine Triphosphate (GTP), respectively. The net reaction is, therefore, thermodynamically favorable, for it results in a lower free energy for the final products.[6] A catabolic pathway is an exergonic system that produces chemical energy in the form of ATP, GTP, NADH, NADPH, FADH2, etc. from energy containing sources such as carbohydrates, fats, and proteins. The end products are often carbon dioxide, water, and ammonia. Coupled with an endergonic reaction of anabolism, the cell can synthesize new macromolecules using the original precursors of the anabolic pathway.[7] An example of a coupled reaction is the phosphorylation of fructose-6-phosphate to form the intermediate fructose-1,6-bisphosphate by the enzyme phsophofructokinase accompanied by the hydrolysis of ATP in the pathway of glycolysis. The resulting chemical reaction within the metabolic pathway is highly thermodynamically favorable and, as a result, irreversible in the cell.[8]

{\displaystyle Fructose-6-Phosphate+ATP\longrightarrow Fructose-1,6-Bisphosphate+ADP}{\displaystyle Fructose-6-Phosphate+ATP\longrightarrow Fructose-1,6-Bisphosphate+ADP}

Cellular respiration

Main article: Cellular respiration

A core set of energy-producing catabolic pathways occur within all living organisms in some form. These pathways transfer the energy released by breakdown of nutrients into ATP and other small molecules used for energy (e.g. GTP, NADPH, FADH). All cells can perform anaerobic respirationby glycolysis. Additionally, most organisms can perform more efficient aerobic respiration through the citric acid cycle and oxidative phosphorylation. Additionally plants, algae and cyanobacteria are able to use sunlight to anabolically synthesize compounds from non-living matter by photosynthesis.

Gluconeogenesis Mechanism

Anabolic pathway (anabolism)

In contrast to catabolic pathways, are the anabolic pathways that require an input of energy in order to conduct the construction of macromolecules such as polypeptides, nucleic acids, proteins, polysaccharides, and lipids. The isolated reaction of anabolism is unfavorable in a cell due to a positive Gibbs Free Energy (+ΔG); thus, an input of chemical energy through a coupling with an exergonic reaction is necessary.[9] The coupled reaction of the catabolic pathway affects the thermodynamics of the reaction by lowering the overall activation energy of an anabolic pathway and allowing the reaction to take place.[10] Otherwise, an endergonic reaction is non-spontaneous.

An anabolic pathway is a biosynthetic pathway, meaning that it combines smaller molecules to form larger and more complex ones.[11] An example is the reversed pathway of glycolysis, otherwise known as gluconeogenesis, which occurs in the liver and sometimes in the kidney in order to maintain proper glucose concentration in the blood and to be able to supply the brain and muscle tissues with adequate amount of glucose. Although gluconeogenesis is similar to the reverse pathway of glycolysis, it contains three distinct enzymes from glycolysis that allow the pathway to occur spontaneously.[12] An example of the pathway for gluconeogenesis is illustrated in the image titled “Gluconeogenesis Mechanism“.